Mild heat shock may be induced in skin as a result of the skin temperature rising to about 45.degree. C. and during conditions of oxidative stress and leads to induction of heat shock protein (or stress protein) formation. The heat shock response is regarded as a survival strategy which serves to protect living cells against temperature and other stresses. It is known that hydrogen peroxide is able to induce the heat shock response (Burdon R H, Gill V, & Rice Evans C. Active oxygen species and heat shock protein induction. In: Stress Proteins. Induction and function. pp. 19-25. Schlesinger M J, Santoro M G, & Garaci E (Eds). Springer-Verlag, Berlin, 1990) and also to generate oxidative stress. It is also known that prostaglandins can induce heat shock protein formation (Santoro M G, Garaci E, & Amici C. Induction of HSP70 by prostaglandins. In: Stress Proteins. Induction and function. pp. 27-44. Schlesinger M J, Santoro M G, & Garaci E (Eds). Springer-Verlag, Berlin, 1990).
Oxidative stress is a perturbation of redox homeostasis in favor of higher levels of oxidizing species relative to reducing species and is essentially a shift in the thiol/disulfide status of tissue biochemistry in favor of higher levels of disulfides.
Materials for inducing heat shock, such as hydrogen peroxide and polymeric materials capable of generating hydrogen peroxide, have previously been used for wound healing. In non-healing wounds, high levels of hydrogen peroxide (in the range of 10.sup.-6 M to about 1M) may serve to initiate the inflammatory phase of wound healing during which wound debris is removed. Low levels of hydrogen peroxide (around 10.sup.-8 M to 10.sup.-6 M) are capable of stimulating fibroblast proliferation during later reconstructive stages of wound healing.
The allergic contact dermatitis reaction is however distinct from the wound healing reaction. Allergic contact dermatitis is regarded essentially as a response arising initially from the activity of antigen-presenting cells and subsequently from the activities of T cells when altered (or foreign) protein is detected by the immune system. Although this may lead to a visible inflammatory and eczematous or bullous reaction, soft tissue breakdown and ulcer formation to form a wound is an occasional but not an inevitable outcome. In contrast, a wound may be regarded as a lesion arising directly from soft tissue breakdown.
Allergic contact dermatitis can be either an acute or chronic eruption, and currently available therapy is varied according to the nature of the eruption.
Current methods of treatment of acute allergic contact dermatitis can involve any of the following: application of cool water, Burrow's solution (typically for 5 to 10 minutes every two to four hours), calamine lotion, topical application of fluorinated corticosteroids in a gel base, systemic corticosteroids (such as ACTH-gel, about 80 units being given intramuscularly followed by at least one further such injection), or a prescribed course of corticosteroid tablets such as dexamethasone.
Chronic allergic contact dermatitis is generally treated by application of topical corticosteroids, such as triamcinolone acetonide followed by less potent corticosteroids such as hydrocortisone or desonide. Chronic hand eczema can also be treated by Grenz ray.
The above do not however provide satisfactory therapeutic treatment of allergic contact dermatitis, and it is an object of the present invention to provide an improved method and formulation for the treatment of allergic contact dermatitis.